This invention relates to plant disease resistance, in particular to plant genes conferring pathogen resistance.
Whether a plant is resistant or susceptible to attack by a given pathogen is frequently under the control of a single, dominant resistance gene (Flor, Annu. Rev. Phytopathol. 9:275-296, 1971). Resistance gene products are thought to recognize signal molecules produced by the pathogen and respond by initiating rapid changes in host cell physiology and metabolism that directly inhibit pathogen growth.
A well-studied model for interactions of plant pathogens with their hosts is that between tomato (Lycopersicon esculentum) and Pseudomonas syringae pv. tomato (Pst; Carland and Staskawicz, Mol. Gen. Genet. 239:17-27, 1993; Martin et al., Mol. Plant-Microbe Interact. 6:26-34, 1993). Two genes required for the tomato signaling pathway that leads to resistance to Pst strains that express the avirulence gene avrPto (Ronald et al., J. Bacteriol. 174:1604-1611, 1992; Salmeron and Staskawicz, Mol. Gen. Genet. 239:6-16, 1993) have been identified through analyses of naturally-occurring resistant and susceptible tomato lines (Pitblado and MacNeill, Canad. J. Plant Pathol. 5:251-255, 1983) and by mutational studies (Salmeron et al., Plant Cell 6:511-520, 1994).
The Pto gene (Pitblado and MacNeill, Canad. J. Plant Pathol. 5:251-255, 1983) encodes a serine/threonine protein kinase with a potential amino-terminal myristoylation site (Martin et al., Science 262:1432-1436, 1993) that lacks additional motifs such as a leucine-rich repeat. Pto is a member of a tightly clustered family of five genes located on the short arm of chromosome five. It encodes a protein highly similar to the cytoplasmic domain of the Brassica self-incompatibility gene SRK and the mammalian signaling factor Raf (Martin et al., Science 262:1432-1436, 1993).
The identification of Pto as a protein kinase suggests that intracellular phosphorylation events are important in the response of tomato to pathogen strains expressing avrPto. The tomato Ptil protein is a substrate for Pto (Zhou et al., Cell 83:925-935, 1995) and Ptil itself is predicted to be a serine/threonine protein kinase (Zhou et al., Cell 83:925-935, 1995). Therefore, the pathway for defense against Pst may incorporate a protein kinase cascade similar to those employed in numerous other eukaryotic signaling pathways (Hunter, Cell 80:225-236, 1995).
The second gene required for resistance of tomato to Pst, designated Prf, was identified through a mutational approach and shown to be tightly linked to Pto (Salmeron et al., Plant Cell 6:511-520, 1994). Analysis of prf mutant alleles suggested that in addition to its role in disease resistance, the Prf protein also functions in the response of tomato to the organophosphate insecticide Fenthion (Salmeron et al., Plant Cell 6:511-520, 1994), a trait that co-segregates with Pto in genetic crosses (Carland and Staskawicz, Mol. Gen. Genet. 239:17-27, 1993). In sensitive tomato lines, Fenthion induces rapid necrosis that mimics the hypersensitive response observed after inoculation with Pst strains expressing avrPto (Laterrot and Philouze, Tomato Genet. Research Coop. Newsletter 35:6, 1985). This observation suggests that Fenthion mimics an elicitor produced under control of the avrPto gene in Pst.
Necrosis in response to Fenthion does not appear to require the Pto kinase (Martin et al., Science 262:1432-1436, 1993; Salmeron et al., Plant Cell 6:511-520, 1994), but rather is conferred by another member of the Pto gene cluster, designated Fen. Fen encodes a protein kinase 80% identical in amino acid sequence to Pto (Martin et al., Plant Cell 6:1543-1552, 1994; Rommens et al., Plant Cell 7:249-257, 1995). Thus, Prf is involved with two similar but distinct kinases, Pto and Fen, to induce hypersensitive-like necrosis in response to pathogen elicitor and Fenthion signals, respectively.